Mitigation of postnatal ethanol-induced neuroinflammation ameliorates trace fear memory deficits in juvenile rats
| Autor: | Derick H. Lindquist, Molly J. Goodfellow, Youn Ju Shin |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty medicine.medical_treatment Inflammation Ibuprofen Hippocampus 03 medical and health sciences Behavioral Neuroscience chemistry.chemical_compound 0302 clinical medicine Internal medicine Conditioning Psychological medicine Hippocampus (mythology) Animals Rats Long-Evans Fear conditioning Neuroinflammation Memory Disorders Ethanol Anti-Inflammatory Agents Non-Steroidal Brain Fear Rats Disease Models Animal 030104 developmental biology Endocrinology Cytokine chemistry Fetal Alcohol Spectrum Disorders Cytokines Tumor necrosis factor alpha medicine.symptom Psychology Neuroscience 030217 neurology & neurosurgery medicine.drug |
| Zdroj: | Behavioural brain research. 338 |
| ISSN: | 1872-7549 |
| Popis: | Impairments in behavior and cognition are common in individuals diagnosed with fetal alcohol spectrum disorders (FASD). In this study, FASD model rats were intragastrically intubated with ethanol (5 g/kg/day; 5E), sham-intubated (SI), or maintained as naive controls (NC) over postnatal days (PD) 4–9. Ethanol exposure during this human third trimester-equivalent period induces persistent impairments in hippocampus-dependent learning and memory. The ability of ibuprofen (IBU), a non-steroidal anti-inflammatory drug, to diminish ethanol-induced neuroinflammation and rescue deficits in hippocampus-dependent trace fear conditioning (TFC) was investigated in 5E rats. Phosphate buffered saline vehicle (VEH) or IBU was injected 2 h following ethanol exposure over PD4-9, followed by quantification of inflammation-related genes in the dorsal hippocampus of PD10 rats. The 5E-VEH rats exhibited significant increases in Il1b and Tnf , but not Itgam or Gfap , relative to NC, SI-VEH, and 5E-IBU rats. In separate groups of PD31-33 rats, conditioned fear (freezing) was significantly reduced in 5E-VEH rats during TFC testing, but not acquisition, compared to SI-VEH and, critically, 5E-IBU rats. Results suggest neuroimmune activation in response to ethanol within the neonate hippocampus contributes to later-life cognitive dysfunction. |
| Databáze: | OpenAIRE |
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